Experimental studies showed that TLR4 expression was significantly elevated in the prefrontal cortex, hippocampus and cerebral cortex in a rat model of the KA-induced epilepsy, and the overexpressed TLR4 exacerbated the neuroinflammation through the following pathways: on the one hand, it directly activated the NF-κB signaling pathway to promote the transcriptional expression of pro-inflammatory factors; on the other hand, it mediated the activation of the MAPK signaling pathway through the Ca2+ influx. The gene discussed is NFKB1; the disease is epilepsy.